APOE ε4 has been the most convincing genome wide signal in AD, and variants in APOE-APOC1-APOC4-APOC2 and TOMM40-APOE have previously been associated with total cholesterol, LDL cholesterol, and triglyceride concentrations.[29, 30] Cholesterol metabolism was implicated to be enriched in the etiology of AD in previous study.[31] In the INRICH analysis, miR-33 targets are enriched in CSF GWAS analysis and miR-33 is critical in regulating cholesterol metabolism, affirming the interrelationship between cholesterol metabolism and AD process. The gene discussed is APOC2; the disease is Alzheimer disease.